ArticleJournal of investigative medicine : the official publication of the American Federation for Clinical Research2013
Activation of carbohydrate response element-binding protein by ethanol.
Article in Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 49 citations in OpenAlex.
- Key Transcription Factors: Avenue for Treating Alcoholic Liver Disease.Current medical science · 2025Review
- Elevated systemic total bile acids escalate susceptibility to alcohol-associated liver disease.iScience · 2024Article
- Glycolytic enzymes in non-glycolytic web: functional analysis of the key players.Cell biochemistry and biophysics · 2024Review
- Interaction of genetic variation at ADH1B and MLXIPL with alcohol consumption for elevated serum urate level and gout among people of European ethnicity.Arthritis research & therapy · 2024Article
- ChREBP is activated by reductive stress and mediates GCKR-associated metabolic traits.Cell metabolism · 2024Article
- Pathogenic mechanisms and regulatory factors involved in alcoholic liver disease.Journal of translational medicine · 2023Review
- Review
- Role of the AMPK/SIRT1 pathway in non‑alcoholic fatty liver disease (Review).Molecular medicine reports · 2023Review
- Therapeutic targets in alcohol-associated liver disease: progress and challenges.Therapeutic advances in gastroenterology · 2023Review
- Ethanol promoting the upregulation of C-X-C Motif Chemokine Ligand 1（CXCL1） and C-X-C Motif Chemokine Ligand 6（CXCL6） in models of early alcoholic liver disease.Bioengineered · 2022Article
- PHLPP1 promotes neutral lipid accumulation through AMPK/ChREBP-dependent lipid uptake and fatty acid synthesis pathways.iScience · 2022Article
- Pathogenesis of Alcohol-Associated Fatty Liver: Lessons From Transgenic Mice.Frontiers in physiology · 2022Review
- The Pentose Phosphate Pathway Dynamics in Cancer and Its Dependency on Intracellular pH.Metabolites · 2020Review
- Current Management and Future Treatment of Alcoholic Hepatitis.Gastroenterology & hepatology · 2020Article
- Alcohol effects on hepatic lipid metabolism.Journal of lipid research · 2020Review
- The Protective Role of the Carbohydrate Response Element Binding Protein in the Liver: The Metabolite Perspective.Frontiers in endocrinology · 2020Review
- Effect of ethanol on lipid metabolism.Journal of hepatology · 2019Review
- Lipophagy and Alcohol-Induced Fatty Liver.Frontiers in pharmacology · 2019Review
- Dietary Macronutrient Composition Determines the Contribution of DGAT1 to Alcoholic Steatosis.Alcoholism, clinical and experimental research · 2018Article
- Role of Nutrition in Alcoholic Liver Disease: Summary of the Symposium at the ESBRA 2017 Congress.Biomolecules · 2018Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveCarbohydrate response element-binding protein (ChREBP) is a transcription factor involved in hepatic lipogenesis. Its function is in part under the control of AMP-activated protein kinase (AMPK) and protein phosphatase 2A (PP2A). Given known effects of ethanol on AMPK and PP2A, it is plausible that ethanol might enhance fatty acid synthesis by increasing the activity of ChREBP. We hypothesized that another potential pathway of ethanol-induced hepatic steatosis is mediated by activation of ChREBP.
methodsThe effects of ethanol on ChREBP were assessed in hepatoma cells and in C57BL/6J mice fed with the Lieber-DeCarli diet.
resultsWhen the cells were exposed to ethanol (50 mM) for 24 hours, the activity of a liver pyruvate kinase (LPK) promoter-luciferase reporter was increased by ∼4-fold. Ethanol feeding of mice resulted in the translocation of ChREBP from cytosol to the nucleus. Protein phosphatase 2A activity was increased in the liver of ethanol-fed mice by 22%. We found no difference in the levels of hepatic Xu-5-P between ethanol-fed mice and controls. Transfection of a constitutively active AMPK expression plasmid suppressed the basal activity of the LPK luciferase reporter and abolished the effect of ethanol on the reporter activity. However, transfection of rat hepatoma cells with a dominant-negative AMPK expression plasmid induced basal LPK luciferase activity by only ∼20%. The effect of ethanol on ChREBP was attenuated in the presence of okadaic acid, an inhibitor of PP2A.
conclusionsThe effects of ethanol on AMPK and PP2A may result in activation of ChREBP, providing another potential mechanism for ethanol-induced hepatic steatosis. However, additional okadaic acid-insensitive effects appear to be important as well.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.